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Journal of Clinical Oncology, Vol 26, No 27 (September 20), 2008: pp. 4515 © 2008 American Society of Clinical Oncology. DOI: 10.1200/JCO.2008.18.6452
In ReplyDivision of General Surgery, Mayo Clinic Cancer Center, Rochester, MN
Division of Medical Oncology, Mayo Clinic Cancer Center, Rochester, MN
Division of Anatomic Pathology, Mayo Clinic Cancer Center, Rochester, MN
Division of Biostatistics, Mayo Clinic Cancer Center, Rochester, MN We are pleased to see that our recent publication on breast cancer risk in women with atypical hyperplasia has elicited additional interest in this subject. Mascarel et al report a lower absolute risk of subsequent breast cancer in a series of 2,833 surgical biopsies performed from 1975 to 2003 for suspicious mammographic microcalcifications than we found in our cohort of women with atypical hyperplasia. They report a 5-year risk of 2.8% (95% CI, 1.4% to 5.5%) and 10-year risk of 5.5% (95% CI, 3.3% to 9.9%) for those found to have epithelial atypia in their group. In the Mayo cohort, we reported a risk of 3.7% (95% CI, 1.6% to 5.8%) at 5 years and 10.9% (95% CI, 7.3% to 14.4%) at 10 years. Mascarel et al suggested two factors that might explain the higher risk reported in our series: (1) inadequate pathologic sampling of biopsy tissues, such that cancers present in the biopsy tissue were not discovered, and (2) inadequate targeting of the highest-risk breast tissues for biopsy because of lack of mammographic screening in early years of the cohort, such that cancers in other areas of the breast were missed/not biopsied. They express their opinion that epithelial atypia is more likely a risk marker of concomitant rather than subsequent cancer. We have concern that what Mascarel et al designate as epithelial atypia may not coincide with atypical hyperplasia as defined for our cohort, in which we used the criteria of Page et al.1 Mascarel et al report finding ductal and/or lobular atypia without concomitant cancer in 670 (24%) of 2,833 of surgical biopsies performed for microcalcifications without a palpable mass. This rate of atypia is at least 10-fold higher than the proportion of patients found to have atypical hyperplasia in another large series of mammographically detected lesions2 and suggests that their patients with "epithelial atypia" are different than our patients reported as atypical hyperplasia. Cases that demonstrate only one histologic feature of epithelial atypia—for instance, either cytologic or architectural atypia—do not constitute a diagnosis of atypical hyperplasia and thus would not be expected to have as high a risk of subsequent breast cancer. According to their concern regarding inadequate sampling of biopsy tissues, cancers already present might have been missed diagnostically. If so, then the subsequent breast cancer risk in our cohort should occur primarily in the ipsilateral breast. Although we found slightly more cancers in the ipsilateral breast than the contralateral breast in our patients with atypia (relative risk = 1.38; 95% CI, 0.79 to 2.21), the difference was not statistically significant. Furthermore, in biomarker investigations in this cohort, we have cut deeper into the blocks for 318 of our 331 women (15 slides of 5-µm each). In so doing, only one case was identified as having a small focus of (invasive) cancer that was not seen on the initial diagnostic histology. In terms of the question of mammographically directed biopsy versus not, we found no difference in breast cancer risk for women with atypical hyperplasia based on the indication for biopsy (ie, mammographic abnormality v palpable concern, P = .72 by Cox proportional hazards regression). Finally, if Mascarel et al are correct and atypical hyperplasia is really a risk marker of concomitant rather than subsequent breast cancer, then we would expect to see an early increase in risk as occult cancers become clinically apparent, with a plateau effect after several years. In fact we saw just the opposite, with little increase in risk in the first 5 years followed by more dramatic increases from years 5 through 15, and no plateau in the increase in breast cancer risk after benign biopsy demonstrating atypical hyperplasia. In summary, our report on atypical hyperplasia is based on the diagnostic criteria of Page et al,1 rather than isolated features of either cytologic or architectural atypia. This likely accounts for the higher breast cancer risk observed in our cohort compared with that of Mascarel et al. We have evidence that our biopsy tissues were sampled appropriately and that the breast cancer risk associated with atypical hyperplasia is not related to the indication for biopsy (ie, mammographic v palpable). We continue to maintain the view that atypical hyperplasia is a marker of subsequent breast cancer risk that applies to both breasts, and this risk persists for at least 15 years after the diagnostic biopsy. AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest. REFERENCES 1. Page DL, Rogers LW: Combined histologic and cytologic criteria for the diagnosis of mammary atypical ductal hyperplasia. Hum Pathol 23:1095-1097, 1992[CrossRef][Medline] 2. Foster MC, Helvie MA, Gregory NE, et al: Lobular carcinoma in situ and atypical lobular hyperplasia at core-needle biopsy: Is excisional biopsy necessary? Radiology 231:813-819, 2004
Related Correspondence
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Copyright © 2008 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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